🎯 Drug Targets

Direct LAMP1 modulators enhance lysosomal membrane trafficking and autophagy flux, while indirect pathway drugs alter lysosomal pH and autophagosome-lysosome fusion dynamics to modulate LAMP1-mediated cellular clearance mechanisms.

Drugs targeting ZO1 typically work by stabilizing or modulating tight junction protein interactions, either by directly binding to ZO1 scaffolding domains or by regulating upstream signaling pathways that control ZO1 phosphorylation and localization. These approaches aim to restore blood-brain barrier integrity or modulate paracellular permeability depending on therapeutic context.

Drugs targeting OCLN would stabilize or enhance tight junction protein interactions, reinforcing the structural integrity of the blood-brain barrier and reducing pathological barrier permeability. Therapeutic approaches would involve either direct protein stabilization or indirect modulation of occludin phosphorylation and trafficking to maintain barrier function.

Targeting protein-heparan sulfate interactions or enzymatic modification

Protein cleavage by botulinum toxin or small molecule modulators of SNARE complex formation

Drug candidates would modulate FLOT1-mediated lipid raft organization and signaling platform assembly, thereby disrupting pathological protein trafficking and reducing amyloid-beta or tau-related pathology in neurodegenerative diseases. FLOT1 inhibitors would interfere with membrane scaffold formation necessary for aberrant signaling in neuroinflammatory and proteinopathic cascades.

No established drugging mechanism for structural membrane protein